Evidence map›Paper›PMID 31413530›Full record

ArticleWorld journal of gastroenterology2019

Berberine prevents stress-induced gut inflammation and visceral hypersensitivity and reduces intestinal motility in rats.

Zhi-Chao Yu, Yong-Xin Cen, Ben-Hua Wu, Cheng Wei, Feng Xiong, De-Feng Li, Ting-Ting Liu, Ming-Han Luo, Li-Liangzi Guo, Ying-Xue Li and 3 more

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Frontiers in pharmacology · 2026
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  20. Potential neuro-immune therapeutic targets in irritable bowel syndrome.Therapeutic advances in gastroenterology · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 1 country.

Zhi-Chao YuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Yong-Xin CenDepartment of Gastroenterology, Foshan Gaoming Affiliated Hospital of Guangdong Medical University, Foshan 528500, Guangdong Province, China.
Ben-Hua WuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Cheng WeiDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Feng XiongDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
De-Feng LiDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Ting-Ting LiuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Ming-Han LuoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Li-Liangzi GuoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Ying-Xue LiDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Li-Sheng WangDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China.
Jian-Yao WangDepartment of General Surgery, Shenzhen Children's Hospital, Shenzhen 518026, Guangdong Province, China.
Jun YaoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen 518020, Guangdong Province, China. yj_1108@126.com.
Shenzhen Second People's Hospital · CNJinan University · CNFoshan Hospital of TCM · CNShenzhen Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIrritable bowel syndrome (IBS) is a common chronic non-organic disease of the digestive system. Berberine (BBR) has been used to treat patients with IBS, but the underlying therapeutic mechanism is little understood. We believe that BBR achieves its therapeutic effect on IBS by preventing stress intestinal inflammation and visceral hypersensitivity and reducing bowel motility.

aimTo test the hypothesis that BBR achieves its therapeutic effect on IBS by preventing subclinical inflammation of the intestinal mucosa and reducing visceral hypersensitivity and intestinal motility.

methodsIBS was induced in rats

resultsWAS led to mucosal inflammation, visceral hyperalgesia, and high intestinal motility. Oral administration of BBR inhibited the NF-κB signal transduction pathway, reduced the expression of pro-inflammatory cytokines [interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α], promoted the expression of anti-inflammatory cytokines (IL-10 and transforming growth factor-β), and improved the terminal ileum tissue inflammation. BBR inhibited the expression of BDNF, TrkB, and C-kit in IBS rats, leading to the reduction of intestinal motility and visceral hypersensitivity. The therapeutic effect of BBR at a high dose (100 mg/kg) was superior to than that of the low-dose (25 mg/kg) group.

conclusionBBR reduces intestinal mucosal inflammation by inhibiting the intestinal NF-κB signal pathway in the IBS rats. BBR reduces the expression of BDNF, its receptor TrkB, and C-kit. BBR also reduces intestinal motility and visceral sensitivity to achieve its therapeutic effect on IBS.

Indexed as

AnimalsBerberineCytokinesDisease Models, AnimalEnteric Nervous SystemGastrointestinal MotilityHumansHyperalgesiaIntestinal MucosaIrritable Bowel SyndromeMaleRatsStress, PsychologicalTreatment OutcomeBerberineCytokinesBerberineBrain-derived neurotrophic factorCajal mesenchymal cellsC-kitIrritable bowel syndromeNuclear factor kappa-BRifampicinVisceral hypersensitivity

Identifiers

PMID31413530
PMCPMC6689801
OpenAlexW2965702766

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.